Fig. 1

Synovitis in rheumatoid arthritis and psoriatic arthritis. Synovitis in rheumatoid arthritis (RA) and psoriatic arthritis (PsA) is triggered by unknown event(s). It is thought that a genetic predisposition and/or environmental cues trigger inappropriate activation of synoviocytes, thereby promoting an autoimmune inflammatory response. Once activated, synoviocytes produce proinflammatory cytokines that in turn activate proximal cells, including endothelial cells that line the blood vessels supplying the joint. This results in dysregulated angiogenesis and the increased infiltration of leukocytes, including monocytes, macrophages, neutrophils, mast cells, eosinophils, B cells and T cells. Infiltrating cells produce cytokines that act in synergy to propagate the inflammatory response. Importantly, tumour necrosis factor alpha (TNFα) and interleukin (IL)-17 are cytokines with major implied roles in PsA and RA pathogenesis and represent important therapeutic targets. With the development of a chronic inflammatory response, the synovial lining becomes hyperplastic. Fibroblasts and macrophages form an invasive matrix (pannus) that promotes the destruction of cartilage and bone. Activation of osteoclast cells promotes bone resorption whereas activation of osteoblasts promotes bone proliferation